Proteasom-Inhibitoren

Zavrski, Ivana; Jakob, Christian; Fleissner, Claudia; Heider, Ulrike; Possinger, K.; Sezer, O.

doi:10.1007/s00761-003-0565-3

Cited by 3 publications

(3 citation statements)

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“…Da in malignen Zellen höhere intrazelluläre Proteasomspiegel gefunden wurden als in normalen Zellen, geht man davon aus, dass die erhöhte proteasomale Aktivität in Tumorzellen den Ablauf der Zellzyklusphasen fördert und damit zur Proliferation beiträgt [27].…”

Section: Proteasominhibitionunclassified

Zielgerichtete Therapie bei soliden Tumoren und in der Hämatoonkologie

et al. 2006

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The development and clinical introduction of targeted therapies has resulted in significant progress for the treatment of malignant diseases. These forms of therapy supplement traditional methods of chemotherapy, radiation, and surgery. As new therapies increase the complexity of therapeutic options in oncology, the treatment costs steadily climb as well. Parameters need to be identified which will predict a response to new substances, and this effort is the subject of ongoing studies.

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Section: Proteasominhibitionunclassified

Zielgerichtete Therapie bei soliden Tumoren und in der Hämatoonkologie

et al. 2006

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“…The primary cause of PMO is decreased estrogen level, which leads to an imbalance between bone resorption and formation (de Boissieu & Trenque, 2017;Meunier et al, 1999;Seven et al, 2016). Abnormal differentiation of bone marrow stromal cells, which leads to reduced numbers of intraosseous osteoblasts and increased adipocytes, and subsequently caused PMO (Zavrski et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Involvement of circRNA_0007059 in the regulation of postmenopausal osteoporosis by promoting the microRNA‐378/BMP‐2 axis

Liu

Wang

Bai

et al. 2020

Cell Biology International

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Increasing evidence suggests that postmenopausal osteoporosis (PMO), a severe disturbance, imposes heavy physical, psychosocial, and financial burdens and dramatically influences the quality of life of postmenopausal women. Circular RNAs (circRNAs) and microRNAs (miRs) play important roles in the occurrence and development of PMO. However, the roles of circRNAs and miRs in osteoporosis regulation still need to be further investigated. circRNAs with different expression levels in patients with PMO were screened via RNA‐seq and bioinformatics analysis. We found that circ_0007059 was upregulated in patients with PMO and during osteoclastogenesis of human bone marrow stromal cells (hBMSCs). Next, we investigated the effect of circ_0007059 overexpression during osteoclastogenesis of hBMSCs. circ_0007059 overexpression attenuated hBMSC differentiation into osteoclasts in vitro. This was demonstrated by downregulated bone morphogenetic protein 2 (BMP‐2) expression, upregulated osteoclast‐specific gene expression, and TRAP staining. circ_0007059 was demonstrated to directly target miR‐378, which in turn targeted BMP‐2 via bioinformatics analysis and the dual‐luciferase reporter assay. Transfection of the miR‐378 mimic reversed the effect of circ_0007059 on the osteoclastogenesis of hBMSCs. These results suggest that circ_0007059 plays an important role in osteoclastogenesis via the miR‐378/BMP‐2 signaling pathway. Targeting the circ_0007059/miR‐378/BMP‐2 axis is possibly a novel idea in osteoporosis treatment.

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“…Es wird vermutet, dass die vermehrte Aktivität des Enzymkomplexes in Tumorzellen den Zellzyklus beschleunigt und damit die Proliferation fördert. Zudem ist eine erhöhte proteosomale Aktivität offenbar an der malignen Transformation hämatopoetischer Zellen beteiligt [6]. Wird das Proteasom pharmakologisch durch einen Proteasominhibitor gehemmt, wird der Stoffwechsel der Tumorzellen unterbrochen und es kommt zur Arretierung der Zelle mit daraus folgender induzierter Apoptose.…”

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PharmaForum

2016

Oncol Res Treat

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Proteasom-Inhibitoren

Cited by 3 publications

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Zielgerichtete Therapie bei soliden Tumoren und in der Hämatoonkologie

Zielgerichtete Therapie bei soliden Tumoren und in der Hämatoonkologie

Involvement of circRNA_0007059 in the regulation of postmenopausal osteoporosis by promoting the microRNA‐378/BMP‐2 axis

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